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| 1 | Cationic nanocarriers induce cell necrosis through impairment of Na^+/K^+-ATPase and cause subsequent inflammatory response显示文摘有积极表面费用的 Nanocarriers 以他们限制了他们的临床的应用的毒性著名。位于他们的毒性下面的机制例如煽动性的反应的正式就职,仍然保持大部分未知。在我们发现了 cationic nanocarriers 的那注射的现在的学习,包括 cationic liposomes, PEI,和 chitosan,导致了坏死的房间的快速的外观。cationic nanocarriers 导致的房间坏死依赖于他们的积极表面费用,但是不要求 RIP1 和 Mlkl。相反,细胞内部的 Na + 超载被发现伴随房间死亡。在文化媒介或有 Na +/K+-ATPase 阳离子绑定地点禁止者 ouabain 的房间的预告的处理的 Na + 的弄空,从房间坏死的保护的房间。而且,有 cationic nanocarriers 的处理在 vitro 并且在 vivo 禁止了 Na +/K+-ATPase 活动。计算模拟证明 cationic 搬运人能与 Na +/K+-ATPase 的阳离子绑定地点交往。有 ouabain 的小剂量的老鼠 pretreated 在 cationic nanocarriers 的致命的剂量的注射以后显示出改进幸存。进一步的分析建议 cationic nanocarriers 和 mitochondrial DNA 的产生的漏导致的那房间坏死能在 vivo 触发严重发炎,它被包含 TLR9 并且 MyD88 发信号的一条小径调停。一起拿,我们的结果揭示由此的新奇机制 cationic nanocarriers 通过和 mitochondrial 的随后的暴露的和 Na +/K+-ATPase, 的相互作用导致尖锐房间坏死是的联系损坏的分子的模式调停的一个关键事件煽动性的回答。我们的学习为评估 nanocarriers 的 biocompatibility 并且为药交货设计更好、更安全的有重要含意。 | Xiawei Wei Bin Shao Zhiyao He Tinghong Ye Min Luo Yaxiong Sang Xiao Liang Wei Wang Shuntao Luo Shengyong Yang Shuang Zhang Changyang Gong Maling Gou Hongxing Deng Yinglan Zhao Hanshuo Yang Senyi Deng Chengjian Zhao Li Yang Zhiyong Qian Jiong Li Xun Sun Jiahuai Han Chengyu Jiang Min Wu Zhirong Zhang | 2015 | Cell Research2015，25，2： | 21 |
| 2 | Twist1-induced miR-199a-3p promotes liver fibrosis by suppressing caveolin-2 and activating TGF-βpathway显示文摘The activation of hepatic stellate cells(HSCs)participates in liver fibrosis,and emerging evidences indicate that microRNAs(miRNAs)are abnormally expressed during HSC activation.However,the potential roles of miRNAs in liver fibrosis still remain elusive.Therefore,this study aimed to investigate the role of miR-199a-3p in liver fibrosis and its underlying mechanism.We found that miR-199a-3p expression was dramatically upregulated during HSC activation in vitro,and during liver fibrogenesis in CCl4-treated rats,and its liver expression was increased in the patients with cirrhosis.By the luciferase assay and RT-qPCR,we revealed that the expression of miR-199a-3p in HSCs was driven by the transcription factor Twist1 which could be further induced by TGF-βtreatment.Functional studies showed that inhibition of miR-199a-3p in both human LX2 cells and rat HSCs significantly decreased the expression of fibrotic markers,such as fibronectin and connective tissue growth factor(CTGF),whereas the forced expression of miR-199a-3p exhibited opposite effects,demonstrating the role of miR-199a-3p in promoting HSC activation.Mechanistically,miR-199a-3p plays an important role in TGF-βsignalling pathway activation through targeting CAV2 that negatively regulates the expression of transforming growth factor-beta receptor type I(TGFβRI).Importantly,administration of antagomiR-199a-3p in the CCl4-treated mice significantly ameliorated hepatic fibrosis.In conclusion,Twist1-induced miR-199a-3p mediates the activation of HSCs by suppressing CAV2 expression and subsequently increasing TGFβRI expression to promote TGF-βpathway.Our findings highlight the therapeutic potential of miR-199a-3p for hepatic fibrosis. | Xiaoxue Yang Liping Ma Rong Wei Tinghong Ye JianKang Zhou Maoyao Wen Ruoting Men Rami I.Aqeilan Yong Peng Li Yang | 2020 | Signal Transduction and Targeted Therapy2020，5，1： | 2 |
| 3 | Targeting fibrosis: mechanisms and clinical trials显示文摘Fibrosis is characterized by the excessive extracellular matrix deposition due to dysregulated wound and connective tissue repair response.Multiple organs can develop fibrosis,including the liver,kidney,heart,and lung.Fibrosis such as liver cirrhosis,idiopathic pulmonary fibrosis,and cystic fibrosis caused substantial disease burden.Persistent abnormal activation of myofibroblasts mediated by various signals,such as transforming growth factor,platelet-derived growth factor,and fibroblast growh factor,has been recongized as a major event in the occurrence and progression of fibrosis.Although the mechanisms driving organ-specific fibrosis have not been fully elucidated,drugs targeting these identified aberrant signals have achieved potent anti-fibrotic efficacy in clinical trials.In this review,we briefly introduce the aetiology and epidemiology of several fibrosis diseases,including liver fibrosis,kidney fibrosis,cardiac fibrosis,and pulmonary fibrosis.Then,we summarise the abnormal cells(epithelial cells,endothelial cells,immune cells,and fibroblasts)and their interactions in fibrosis.In addition,we also focus on the aberrant signaling pathways and therapeutic targets that regulate myofibroblast activation,extracellular matrix cross-linking,metabolism,and inflammation in fibrosis.Finally,we discuss the anti-fibrotic drugs based on their targets and clinical trials.This review provides reference for further research on fibrosis mechanism,drug development,and clinical trials. | Manyu Zhao Liqun Wang Mengzhu Wang Shijie Zhou Ying Lu Huijie Cui Alexandra C.Racanelli Ling Zhang Tinghong Ye Bisen Ding Ben Zhang Jinliang Yang Yuqin Yao | 2022 | Signal Transduction and Targeted Therapy2022，7，7： | 1 |
| 4 | Protective effects and microarray-based mechanism of sea cucumber hydrolysates against high-glucose induced nephrotoxicity in mouse glomerulus mesangial cells显示文摘Diabetic nephropathy(DN)is a common type of end-stage renal disease and glomerular mesangial cells(GMCs)are widely used as a cell model for DN.This study firstly investigated the inhibitory effects of the Apostichopus japonicus and Acaudina leucoprocta hydrolysates on cellular growth under high-glucose treatment,better inhibitory effect of A.japonicus hydrolysate was observed compared to that of A.leucoprocta hydrolysate.Subsequently,the global transcription profiles obtained via microarray analysis showed that 6070 and 7015 genes were identified in the A.japonicus and A.leucoprocta groups compared with the model group,respectively.Among them,transcriptions of the slc30a4,slc35dl,tppp3,tp53inpl,bcl-2,apafl,alox12b and adrala genes were restored from the levels of the model group to those of the control group,contributed to cell mitosis and proliferation in both treatment groups.In addition,other apoptosis-related genes,such as bcl-6,clu,foxo3 and akt,showed opposite trends between two groups,which might cause the difference in inhibitory effect.We preliminarily proposed that the regulation effects of A.japonicus and A.leucoprocta on the genes involved in cellular mitosis,proliferation and apoptosis,might contribute to their inhibitory activity on GMCs under high-glucose environment. | Lingxin Geng Jiaojiao Han Jun Zhou Ye Li Tinghong Ming Zhen Zhang Chenyang Lu Xiurong Su | 2024 | Journal of Future Foods2024，4，3： | 0 |
| 5 | A nonenzymatic electrochemical sensor for the detection of hydrogen peroxide in vitro and in vivo fibrosis models显示文摘Fibrosis occurs due to the excessive deposition of extracellular matrix caused by cell injury.After various types of tissue injury,the dysregulation of the internal response can eventually lead to the destruction of organ structure and dysfunction.There is increasing evidence that oxidative stress,which is characterized by excessive production of hydrogen peroxide(H_(2)O_(2)),is an important cause of fibrosis.Therefore,we synthesized a biosensitive and efficient electrochemical H_(2)O_(2)sensor based on PtNi nanoparticle-doped N-reduced graphene oxide(PtNi-N-rGO)to detect H_(2)O_(2)released from transforming growth factorβ1(TGFβ1)-induced myofibroblast.In addition,the sensor could easily detect changes in H_(2)O_(2)in the lung and bronchoalveolar lavage fluid(BALF)of mice with pulmonary fibrosis.Furthermore,the sensor could also detect H_(2)O_(2)in activated hepatic stellate cells and the liver of carbon tetrachloride(CCl_(4))-induced liver fibrosis.Moreover,the alterations in H_(2)O_(2)detected by the sensor were consistent with nicotinamide adenine dinucleotide phosphate oxidase 4(NOX4)protein expression and the staining results of pathological sections.Taken together,these results highlight the use of H_(2)O_(2)sensors for the rapid detection of fibrosis and facilitate the rapid evaluation of antifibrotic drug candidates. | Hongyao Liu Yan Yu Taixiong Xue Cailing Gan Yuting Xie Doudou Wang Peilin Li Zhiyong Qian Tinghong Ye | 2024 | Chinese Chemical Letters2024，35，3： | 0 |
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